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Related Experiment Video

Updated: Apr 18, 2026

Subcellular Imaging of Neuronal Calcium Handling In Vivo

Subcellular Imaging of Neuronal Calcium Handling In Vivo

Published on: March 17, 2023

Bax regulates neuronal Ca2+ homeostasis.

Beatrice D'Orsi¹, Seán M Kilbride¹, Gang Chen¹

¹Department of Physiology and Medical Physics, Centre for the Study of Neurological Disorders and 3U-COEN, Royal College of Surgeons in Ireland, Dublin 2, Ireland; and.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|January 30, 2015

Summary

Bax deficiency protects neurons from excitotoxic injury by regulating calcium signaling, independent of its apoptotic role. Bax-deficient neurons show reduced calcium transients and improved endoplasmic reticulum calcium handling, preventing excitotoxicity-induced neuronal death.

Keywords:

Bcl-2 family protein NMDA cerebral ischemia endoplasmic reticulum excitotoxicity mitochondria

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Area of Science:

Neuroscience
Cell Biology
Molecular Biology

Background:

Excitotoxicity, driven by excessive glutamate receptor activation, causes neuronal death.
Bax protein is a key mediator of apoptosis.

Purpose of the Study:

To investigate the role of Bax in excitotoxicity-induced neuronal death.
To determine if Bax influences calcium (Ca2+) dynamics during excitotoxicity.

Main Methods:

Neuronal cultures and mouse models of stroke (middle cerebral artery occlusion).
Analysis of neuronal Ca2+ transients, mitochondrial membrane potential (Δψm), and intracellular ATP levels.
Use of FRET-based sensors and Ca2+-ATPase inhibitor thapsigargin.

Main Results:

Bax deficiency conferred neuroprotection against excitotoxic injury and stroke.
Bax-deficient neurons exhibited reduced Ca2+ transients and preserved Δψm during excitotoxicity.
Bax influenced Ca2+ signaling independently of its pro-apoptotic function, particularly in endoplasmic reticulum Ca2+ handling.

Conclusions:

Bax plays a critical role in excitotoxicity-induced neuronal death by modulating Ca2+ signaling.
Targeting Bax may offer a neuroprotective strategy against excitotoxic brain injury.